eMedinewS Editorial

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Coffee, Sex, Smog Can All Trigger Heart Attack, Study Finds

Air pollution while stuck in traffic topped the list of potential heart attack triggers, with the researchers pegging 7.4% of heart attacks to roadway smog. Coffee was also linked to 5% of attacks, booze to another 5 percent, and pot smoking to just under 1 percent, the European researchers found. Among everyday activities, exerting yourself physically was linked to 6.2% of heart attacks, indulging in a heavy meal was estimated to trigger 2.7%, and sex was linked to 2.2%.

For example, air pollution is a minor trigger for heart attacks, but since so many people are exposed to smog, it triggers many more heart attacks than other more potent triggers, such as alcohol and cocaine.

The report is published in the Feb. 24 online edition of The Lancet. In terms of risk, the team found that air pollution increased a person’s risk of having a heart attack by just under 5%. In contrast, coffee increased the risk by 1.5 times, alcohol tripled the risk, and cocaine use increased the odds for heart attack 23–fold. However, because only a small number of people in the entire population are exposed to cocaine, while hundreds of millions are exposed to air pollution daily, air pollution was estimated to cause more heart attacks across the population than cocaine.

Even emotional states can sometimes trigger a heart attack, the team found. For example, negative emotions in general were linked to almost 4% of heart attacks while anger, specifically, was linked to just over 3 percent. Even “good” emotional states were tied to 2.4% of heart attacks.
(Source: Medlineplus)

Dr KK Aggarwal
Editor in Chief

eMedinewS Editorial

Health Care 186 Comments

FDA orders new cautions on antipsychotic drugs

All antipsychotic drugs, including older agents as well as second–generation products, must contain new label information regarding their use in pregnancy. In particular, the new labeling will address the risk of extrapyramidal symptoms (EPS) and withdrawal syndromes in newborns.

FDA has updated the Pregnancy section of drug labels for the entire class of antipsychotic drugs to include consistent information about the potential risk for EPS and/or withdrawal symptoms in newborns whose mothers were treated with these drugs during the third trimester of pregnancy. The FDA has identified 69 episodes of neonatal EPS or withdrawal in adverse event reports submitted to the agency through October 2008. Among the symptoms listed in the reports: agitation, hypertonia, hypotonia, tremor, somnolence, respiratory distress, and feeding disorder. Onset of symptoms ranged from birth to one month later, and the severity varied as well.

The FDA indicated that some infants recovered within hours while others needed intensive care and prolonged hospitalization.

Dr KK Aggarwal
Editor in Chief

eMedinewS Editorial

Health Care 179 Comments

NIH–funded study finds new possible risk factor of heart disease

Abnormal heart rate turbulence is associated with an increased risk of heart disease death in otherwise low–risk older individuals, according to a study funded by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health. This study appears in the Feb. 15 edition of the Journal of Cardiovascular Electrophysiology.

Among the nearly 1,300 study participants, heart rate turbulence, which reflects how well the heart reacts to occasional premature contractions, was an even stronger heart disease risk factor than elevated levels of C–reactive protein. CRP is a potential heart disease biomarker that has emerged in recent years.

Study participants considered at low risk of heart disease based on traditional risk factors were on average 8 to 9 times more likely to die of heart disease during the roughly 14–year follow–up period if they had abnormal heart rate turbulence values. Traditional risk factors include age, gender, high blood cholesterol, high blood pressure, obesity, diabetes, and smoking. Low–risk individuals with elevated CRP in their blood were about 2.5 times more likely to die than those with normal or low CRP.

This study followed 1,272 adults aged 65 and older as part of the NHLBI’s Cardiovascular Health Study. Participants were categorized as healthy (no sign of heart disease risk except possibly diabetes), subclinical (some signs of heart disease) or clinical (had a cardiovascular event, such as a heart attack). At the onset, participants underwent 24–hour monitoring of their hearts’ electrical activity through a Holter monitor.

Abnormal heart rate turbulence and CRP levels both appeared to independently correlate with an increased likelihood of dying of heart disease in the group that was categorized as healthy, even after controlling for other risk factors. Abnormal heart rate turbulence — present in about 7 percent of the study participants — also predicted an increased likelihood of heart disease death in the subclinical and clinical groups, though these results were not as pronounced.

Heart rate turbulence refers to how smoothly the heart rate returns to normal after a premature ventricular contraction, a fairly common event in which the second portion of a heart beat is triggered too soon. Due to the improper timing between the atrial and ventricular contractions, the ventricles haven’t fully filled with blood and therefore do not push out enough blood to the body. The brain detects this sub–optimal release of blood and instantly increases the heart rate to pump more blood. However, this overcompensation raises blood pressure, causing the brain to react again and lower the heart rate until blood pressure returns to normal.

By analyzing the heart’s electrical signals, physicians can measure the magnitude of the initial heart rate jump (turbulence onset) and the speed at which heart rate returns to normal (turbulence slope), and then determine if the heart rate turbulence response is normal or abnormal.

A heart rate turbulence measurement is insightful because it offers a sign of how well the autonomic, or subconscious, nervous system is functioning,” said study author Phyllis K. Stein, Ph.D., a research associate professor of medicine and director of the Heart Rate Variability Laboratory at Washington University School of Medicine in St. Louis.

  1. After a VPC, heart rate increases for 1 or 2 beats, then decreases.
  2. This phenomenon was discovered by Georg Schmidt’s research group in Munich, when they averaged the RR interval sequences flanking VPCs
  3. RR interval start to increase at beat 3 after the paced VPC, and reaches a peak bradycardia over the baseline RR at beat 8.
  4. HRT quantifies these heart rate changes by 2 parameters, turbulence onset (TO) and turbulence slope (TS).
  5. TO is the amount of sinus acceleration following a VPC, TS is the rate of sinus deceleration that follows the sinus acceleration.
  6. HRT is measured. RR intervals are plotted vs beat number, with 2 beats preceding and 20 beats succeeding the VPC beat and compensatory pause.
  7. TO (%)= 100 × ((RR (1) + RR (2)) – (RR (–3) + RR (–2))/(RR (–3) + RR (–2)), where the numbers in brackets denote beat number, with the compensatory pause being beat 0.
  8. To obtain TS (ms/beat), the slopes of RR change are calculated by fitting each 5 beat RR sequence following the compensatory pause (RR (1)~RR (5), RR (2)~RR (6), …, RR (16)~RR (20)) with a straight line. The maximum of the 16 slopes is taken to be TS. TO<0 and TS>2.5 are considered normal, TO > 0 and TS < 2.5 are considered abnormal.
  9. In other words, strong sinus acceleration followed by rapid deceleration marks a healthy response.
  10. TO is the difference in the average of the 2 RR intervals preceding and succeeding the VPC/compensatory pause sequence expressed as a percentage.

Dr KK Aggarwal
Editor in Chief

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